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All NTG and R120G TG?�Nico mice tested showed sinus rhythm during ECG recording over a period of 10�min. In addition, ECG recordings for 10�min did not reveal any other arrhythmias in any of the mice in all three groups. Table? gives overall data for electrophysiological parameters in the three groups of mice. All ECG parameters measured, except RR interval and QTc, were prolonged in R120G TG compared with NTG [http://www.selleckchem.com/products/ipi-145-ink1197.html selleck chemical] mice. Interestingly, although the QT interval was still prolonged in R120G TG?�Nico compared with NTG mice, the P and PR intervals and QRS complex had returned to normal in R120G TG?�Nico mice. Moreover, there was no significant difference in QTc among the three groups. Figure?a shows representative examples of monophasic action potentials recorded from the epicardial surface of the posterior left ventricle in the three different groups during steady state pacing [http://en.wikipedia.org/wiki/Alkaline_phosphatase (-)-p-Bromotetramisole Oxalate] at a cycle length of 200�msec. Ventricular monophasic APD prolongation was observed in R120G TG and R120G TG?�Nico hearts compared with NTG hearts. Mean monophasic APD was significantly prolonged in left ventricles from R120G TG and R120G TG?�Nico mice compared with NTG mice at pacing cycle lengths of 200 and 150�msec (Fig.?b). Interestingly, levels of mean monophasic APD were similar among the three groups at a pacing cycle length of 100�msec. Figure?a shows representative examples of activation isochrone [http://www.selleckchem.com/products/JNJ-26481585.html Epigenetics inhibitor] maps recorded from the epicardial surface of the anterior left ventricle during steady state pacing at cycle lengths of 200, 150 and 100�msec in the three groups. Relative crowding of isochrone lines for R120G TG hearts (Fig.?b) indicates conduction slowing compared with NTG and R120G TG?�Nico hearts (Fig.?b). In addition, when considering all experiments (Fig.?b), the mean CV of the left ventricle was significantly slower in R120G TG than NTG hearts, and nicorandil significantly improved the decreased CV in R120G TG hearts. Before rapid pacing, spontaneous VT was not observed in any Langendorff-perfused NTG, R120G TG and R120G TG?�Nico hearts. Rapid pacing induced VT in six of eight R120G hearts (Table?). In contrast, rapid pacing did not induce VT in any NTG and R120G TG?�Nico hearts (Table?). Nicorandil significantly reduced the incidence of VT induction by rapid pacing in R120G TG hearts (P??.05). Figure? shows an example of electrically induced VT in a Langendorff-perfused R120G TG heart. A representative ECG and monophasic action potential signal during VT showed rapid repetitive activation at a cycle length of